Figure 4
Telomere-focused model of tumorigenesis. Dysfunctional telomeres, either as a consequence of telomere decapping or resulting
from telomere shortening, will be recognized by the DNA surveillance machinery and induce senescence or apoptosis (telomeres
are shown as red circles). In the setting of checkpoint deficiency, such as p53 deficiency, chromosomes may fuse and start BFBs, leading to a shuffling of the genome and genomic amplifications and deletions.
This first step generates a pro-cancer genome. In a second step, chromosomes are stabilized by telomere length maintenance
mechanisms (either TA or ALT) and the emerging cancer cells acquire independence of telomere shortening-induced senescence
or apoptosis.